Morel I, Abaléa V, Sergent O, Cillard P, Cillard J
INSERM U456, UFR des Sciences Pharmaceutiques es et Biologiques, Rennes, France.
Biochem Pharmacol. 1998 May 1;55(9):1399-404. doi: 10.1016/s0006-2952(97)00648-5.
Supplementation of rat hepatocyte cultures with the flavonoid myricetin (300 microM) led to the formation of phenoxyl radical intermediates, as detected in intact cells by electron paramagnetic resonance (EPR) spectroscopy. These radicals corresponded to one-electron oxidation products of myricetin. The level of phenoxyl radicals was significantly reduced when myricetin-treated hepatocyte cultures were also supplemented with iron (Fe-NTA 100 microM). This suggested that iron could accelerate the oxidation flux of myricetin. Moreover, myricetin was found to be able to inhibit lipid peroxidation induced by iron in hepatocyte culture. Free malondialdehyde (MDA) levels and the amount of radicals derived from oxidized lipids were greatly reduced when myricetin was added to iron-treated cultures. This showed that myricetin was a good inhibitor of lipid peroxidation in this model and that the intermediate generation of phenoxyl radicals might contribute to the antioxidant mechanism of myricetin.
用黄酮类化合物杨梅素(300微摩尔)补充大鼠肝细胞培养物,会导致苯氧自由基中间体的形成,这通过电子顺磁共振(EPR)光谱在完整细胞中检测到。这些自由基对应于杨梅素的单电子氧化产物。当用杨梅素处理的肝细胞培养物中也补充铁(100微摩尔的Fe-NTA)时,苯氧自由基的水平显著降低。这表明铁可以加速杨梅素的氧化通量。此外,发现杨梅素能够抑制肝细胞培养中铁诱导的脂质过氧化。当将杨梅素添加到经铁处理的培养物中时,游离丙二醛(MDA)水平以及源自氧化脂质的自由基量大大降低。这表明杨梅素在该模型中是脂质过氧化的良好抑制剂,并且苯氧自由基的中间生成可能有助于杨梅素的抗氧化机制。